DCNAS-Net: deformation convolution and neural architecture search detection network for bone marrow oedema.

BACKGROUND: Lumbago is a global disease that affects more than 500 million people worldwide. Bone marrow oedema is one of the main causes of the condition and clinical diagnosis is mainly made by radiologists manually reviewing MRI images to determine whether oedema is present. However, the number of patients with Lumbago has risen dramatically in recent years, which has brought a huge workload to radiologists. In order to improve the efficiency of diagnosis, this paper is devoted to developing and evaluating a neural network for detecting bone marrow edema in MRI images. RELATED WORK: Inspired by the development of deep learning and image processing techniques, we design a deep learning detection algorithm specifically for the detection of bone marrow oedema from lumbar MRI images. We introduce deformable convolution, feature pyramid networks and neural architecture search modules, and redesign the existing neural networks. We explain in detail the construction of the network and illustrate the setting of the network hyperparameters. RESULTS AND DISCUSSION: The detection accuracy of our algorithm is excellent. And its accuracy of detecting bone marrow oedema reached up to 90.6[Formula: see text], an improvement of 5.7[Formula: see text] compared to the original. The recall of our neural network is 95.1[Formula: see text], and the F1-measure also reaches 92.8[Formula: see text]. And our algorithm is fast in detecting it, taking only 0.144 s per image. CONCLUSION: Extensive experiments have demonstrated that deformable convolution and aggregated feature pyramid structures are conducive for the detection of bone marrow oedema. Our algorithm has better detection accuracy and good detection speed compared to other algorithms.

Hyaluronic acid-modified curcumin-copper complex nano delivery system for rapid healing of bacterial prostatitis.

Bacterial prostatitis is a bacterial infection of the prostate gland presenting with lower quadrant abdominal pain, urination disorders and poor fertility. In recent years, reports have emerged on the significantly reduced efficacy of fluoroquinolone drugs attributed to multiple drug-resistant bacteria, emphasizing the need for new drugs. In this study, we designed a targeting drug delivery system via curcumin copper complex grafted with hyaluronic acid. Subsequently, the prepared system was characterized using FT-IR, XRD, SEM, XPS and 1H NMR methods. In addition to the substantial improvement in the solubility of the carrier, its antibacterial performance and targeting ability were improved. Interestingly, the grafting of hyaluronic acid endowed the carrier with excellent CD44 receptor targeting function and good water solubility, and the complexation of copper ions greatly enhanced its antibacterial capability, especially the inhibitory effect on E. coli. The anti-prostatitis effect of the drug was evaluated comprehensively by establishing a bacterial prostatitis model infected by E. coli. Assessment of the anti-prostatitis effects in vivo indicated that the Cur-Cu@HA delivery system could effectively promote recovery from bacterial prostatitis by downregulating inflammation. In conclusion, our Cur-Cu@HA delivery system has great potential for treating bacterial prostatitis.

SOX30, a target gene of miR-653-5p, represses the proliferation and invasion of prostate cancer cells through inhibition of Wnt/ß-catenin signaling.

BACKGROUND: Sex-determining region Y-box containing gene 30 (SOX30) is a newly identified tumor-associated gene in several types of cancer. However, whether SOX30 is involved in the development and progression of prostate cancer remains unknown. This study investigated the potential role of SOX30 in prostate cancer. METHODS: Prostate cancer cell lines and a normal prostate epithelial cell line were used for the experiments. The expression of SOX30 was determined using quantitative real-time PCR and western blot analysis. The malignant cellular behaviors of prostate cancer were assessed using the Cell Counting Kit-8, colony formation and Matrigel invasion assays. The miRNA-mRNA interaction was validated using the dual-luciferase reporter assay. RESULTS: SOX30 expression was lower in cells of prostate cancer lines than in cells of the normal prostate epithelial line. Its overexpression repressed the proliferation and invasion of prostate cancer cells. SOX30 was identified as a target gene of microRNA-653-5p (miR-653-5p), which is upregulated in prostate cancer tissues. MiR-653-5p overexpression decreased SOX30 expression, while its inhibition increased SOX30 expression in prostate cancer cells. MiR-653-5p inhibition also markedly restricted prostate cancer cell proliferation and invasion. SOX30 overexpression or miR-653-5p inhibition significantly reduced ß-catenin expression and downregulated the activation of Wnt/ß-catenin signaling. SOX30 knockdown significantly reversed the miR-653-5p inhibition-mediated inhibitory effect on the proliferation, invasion and Wnt/ß-catenin signaling in prostate cancer cells. CONCLUSIONS: These results reveal a tumor suppressive function for SOX30 in prostate cancer and confirmed the gene as a target of miR-653-5p. SOX30 upregulation due to miR-653-5p inhibition restricted the proliferation and invasion of prostate cancer cells, and this was associated with Wnt/ß-catenin signaling suppression. These findings highlight the importance of the miR-653-5p-SOX30-Wnt/ß-catenin signaling axis in prostate cancer progression.

Suppression of microRNA-454 impedes the proliferation and invasion of prostate cancer cells by promoting N-myc downstream-regulated gene 2 and inhibiting WNT/ß-catenin signaling.

MicroRNA-454 (miR-454) is emerging as critical regulator in tumorigenesis; it may function as an oncogene or a tumor suppressor. However, the role of miR-454 in prostate cancer remains unknown. In this study, we aimed to investigate the function and molecular mechanisms of miR-454 in prostate cancer. We found that miR-454 was highly expressed in prostate cancer tissues and cell lines (*p<0.05), as detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell counting kit-8 assay, colony formation assay and cell invasion assay showed that the inhibition of miR-454 significantly suppressed prostate cancer cell proliferation and invasion (*p<0.05), whereas the overexpression of miR-454 markedly promoted prostate cancer cell proliferation and invasion (*p<0.05). Bioinformatics analysis showed that N-myc downstream-regulated gene 2 (NDRG2), a well-known tumor suppressor, was identified as a potential target gene of miR-454. Dual-luciferase reporter assay showed that miR-454 directly targeted the 3'-untranslated region of NDRG2. RT-qPCR and western blot showed that miR-454 overexpression significantly decreased NDRG2 expression (*p<0.05), whereas miR-454 inhibition markedly promoted NDRG2 expression (*p<0.05). Spearman's correlation analysis showed that miR-454 expression was inversely correlated with NDRG2 expression in prostate cancer tissues (r=-0.8932; p<0.0001). Moreover, miR-454 inhibition significantly suppressed the protein expression of ß-catenin (*p<0.05) and blocked the activation of WNT signaling (*p<0.05). In addition, small interfering RNA mediated NDRG2 knockdown significantly reversed the antitumor effect of miR-454 inhibition on prostate cancer cell proliferation and invasion (*p<0.05). Taken together, these results reveal an oncogenic role of miR-454, which promotes prostate cancer cell proliferation and invasion by downregulation of NDRG2. These results also suggest miR-454 as a potential therapeutic target for the treatment of prostate cancer.